Graves' disease: changes in TSH receptor and anti-microsomal antibodies after thyroidectomy

It has been suggested that intrathyroidal plasma cells are the major site of TSH receptor antibody synthesis in Graves' disease (GD). To investigate this hypothesis, serial serum levels of TSH receptor antibodies, as determined by a recently developed immunoprecipitation assay (IPA), were measured in 13 patients with GD before and after subtotal thyroidectomy (Tx). Pretreatment TSH receptor antibody levels (86.4 +/- 26.8 pM/ml; mean +/- s.d.) decreased significantly due to antithyroid drug therapy to 60.3 +/- 21.5 pM/ml (P less than 0.05) just before Tx. However, 4 h after Tx, there was a significant increase (84.9 +/- 35.5 pM/ml; P less than 0.05) due to leakage of antibodies from the manipulated thyroid gland. After Tx, no major decrease in autoantibody levels occurred; TSH receptor antibodies were still detectable 1 to 7 months after Tx (88.7 +/- 44.6 pM/ml). Neither an acute change nor an overall reduction in anti-microsomal (M) antibody titres was observed after Tx. Our conclusions are that serum TSH antibody levels exhibited a drug-induced decrease before Tx and an immediate, but transient, post-operative increase. The post-operative increase was caused by leakage of preformed TSH receptor antibodies from the manipulated thyroid gland. Several months after Tx, TSH receptor and anti-M antibodies were present in the same serum concentrations as before treatment. The present data does not support the hypothesis that plasma cells in the thyroid gland are the major site of autoantibody synthesis in GD at the time of Tx.